Both chronic hypoxemia and increased airway resistance have been implicated in the etiology of the Sudden Infant Death Syndrome (SIDS). We have found that under hypoxic conditions, kittens may exhibit a respiratory failure syndrome manifested in quiet sleep (QS) and reversed in active sleep (AS). It is hypothesized that the relative immunity of human neonates to SIDS results from the prevalence of AS in young infants whereas vulnerability of older infants is due to increased QS. Exp. 1 would test a hypothesis that vulnerability to hypoxic respiration failure and death is increased in intermediate aged infants. An alternative theory suggests that, during AS, compensation for airway obstruction will be defeated by intercostal EMG depression and chest wall collapse. Exps. 2 and 3 will assess the respiratory responses to hypoxia, chronic partial airway obstruction, and combined hypoxia and airway obstruction during QS and AS in 20 day old kittens. Standardized polygraphic recordings and pneumotachographic measurements will be used to determined sleep state patterns, cardiac and respiratory patterns (including apneas), intrathoracic pressure, ventilation, and laryngeal adductors and diaphragmatic electromyographic activity. Treatment procedures are designed to produce a respiration failure syndrome characterized by apneic patterns. Exp. 4 will use changes in temperature to modify sleep state distribution, in order to further assess the role of sleep states in vulnerability to respiratory failure and to assess the interaction of sleep, thermoregulation, and adaption to hypoxia. Exp. 5 will compare effects of hypoxia since birth and acute hypoxia in terms of standard parameters. Exp. 6 will assess prophylactic effectiveness of a stimulant drug, aminophylline, in terms of both sleep state distribution and respiratory parameters.